Additional pathways include intestinal-barrier reinforcement with reduced endotoxemia and liver inflammation, modulation of SCFA and bile-acid signaling via free fatty acid receptors 2 and 3 (FFAR2/3) and Farnesoid X receptor (FXR)/Takeda G protein-coupled receptor 5 (TGR5), and dipeptidyl peptidase-IV (DPP-IV-inhibitory) or Angiotensin-Converting Enzyme-Inhibitory (ACE-inhibitory) peptides generated during legume and cereal fermentations [32,33,34]. The gene discussed is FFAR2; the disease is serum lipopolysaccharide activity.